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33
Fractures in the Stiff and Osteoporotic Spine

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Oren G. Blam, M.D. Jerome M. Cotler, M.D.

The structural integrity of the spine is a result of bony resistance to failure and of stability afforded by surrounding soft tissues. Disorders that affect these characteristics may produce a stiff and brittle spinal column predisposed to pathologic fracture, in the rst instance by causing a thinning of the bone and in the second by reducing the energy-dissipating capacity of paraspinal ligaments and discs. Postmenopausal and advanced-age osteoporosis, ankylosing spondylitis, diffuse idiopathic skeletal hyperostosis, and other related conditions may predispose the spine to low-energy fracture and result in characteristic injury patterns. These injuries can be difcult to recognize because of the often subacute or chronic nature of neck or back pain in patients with these conditions. The radiographic appearance of the underlying disease state can complicate interpretation of fracture versus chronic changes after trivial trauma. Nevertheless, patients with these injuries are important to recognize because they may be at heightened risk for post-traumatic deformity and for neurologic deterioration, especially after a delay in diagnosis.

OSTEOPOROTIC SPINAL FRACTURES

zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz Osteoporosis is becoming a more common cause of pathologic spinal fracture as population demographics reveal an increasing proportion of people older than age 65. The lifetime risk of a symptomatic vertebral osteoporotic fracture has been reported as 16% for women and 5% for men, with higher frequencies estimated when including asymptomatic fractures. Reported prevalences range from 10% in middle-aged women to 63% in elderly women.28 Osteoporosis is the progressive loss of bone content in the axial and appendicular skeleton, dened as a bone mineral density of less than 2.5 standard deviations below the mean for young, healthy people. Postmenopausal, or type I, osteoporosis results from altered bone turnover
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caused by decreasing circulating estrogen levels. Osteoclastic function increases out of proportion to osteoblastic function. Trabecular bone is affected more than cortical bone because of the greater surface area trabeculae present to osteoclasts for bone degradation. Postmenopausal women (usually older than age 50) are at risk, with higher incidences found for smokers, whites and Asians, women with short or thin builds, those with early menopause, and those with a positive family history of osteoporosis. Advanced-age, or type II, osteoporosis occurs equally in men and women older than age 70 and is caused by decreased osteoblastic bone formation, affecting cortical and trabecular bone equally. In the osteoporotic spine, the vertebral body contains bone voids that can collapse, leading to end-plate scalloping, vertebral wedging, and kyphotic deformity. The cortical shell of the vertebral body contributes only 10% of compressive strength of the centrum,36 and compressive strength of trabecular bone is related to the square of its apparent density.32 Loss of trabecular bone can therefore have a profound effect on compressive strength of the vertebral body. Prevention methods may prove to be most important in managing osteoporotic spinal fracture. Sufcient dietary calcium intake during the rst 25 years of life may be most important because peak lifetime bone mass begins to decline afterward. Further adequate dietary intake of calcium and vitamin D during adulthood may slow this progressive decline; it is recommended that adults ingest 1500 mg of calcium and 800 international units of vitamin D each day.25 People at risk for osteoporosis may be evaluated with bone density tests, the most accurate of which is dual-emission x-ray absorptiometry (DEXA). Medical management of osteoporosis includes dietary supplementation of calcium and vitamin D; antiresorptive agents such as estrogen, calcitonin, and bisphosphonates; and bone-stimulating agents such as uoride. Teaching fall avoidance, proper lifting techniques, and overall body conditioning exercises also is important.25 The upper thoracic spine is the most common site for

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osteoporotic spinal fracture. No antecedent history of trauma may be present, although back pain with tenderness over the spine usually occurs. Radicular pain or neurologic decit may occur acutely. Late development of radicular symptoms or neurologic deterioration weeks after the initiation of spinal pain may also occur because of progressive vertebral collapse with ensuing nerve root impingement or even spinal cord compression. Cord compression is uncommon and usually self-limited.26 Osteoporotic fractures are usually caused by compression forces. Loss of anterior vertebral body height with wedging and kyphotic deformity occurs. Alternatively, the fractured osteoporotic vertebral body may fail at superior and inferior end-plates, resulting in a shortened but trapezoidal shape. Although a low-energy injury, the fracture may rarely propagate through the middle column, resulting in a burst-type fracture pattern (Fig. 331). Plain radiography can delineate the fracture, but posterior cortical involvement with canal encroachment can be better visualized with computed tomography (CT). Radiographic and CT evidence of old, nonacute fractures includes bony sclerosis, rounded edges of the fracture fragments, and bony cyst formation. If the age of the fracture remains indeterminate, a bone scan may be

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FIGURE 331. Osteoporotic burst fracture. Note the greater than 50% collapse of anterior vertebral body height and the involvement of the posterior cortex of the vertebral body.

necessary to decide whether treatment is needed. A positive bone scan represents the presence of attempts at bone healing and may last 18 or more months. Magnetic resonance imaging (MRI) can be useful in the presence of neurologic decit. It is, however, not denitive for differentiating between low-energy compression fractures in osteopenic bone and pathologic fractures caused by metastatic disease, except when a soft tissue mass is present in combination with the metastasis. A short course of analgesia is the mainstay of treatment. Hospital admission is most commonly necessary for older individuals who present to the emergency department with the acute incidence of a low-energy compression fracture. Especially at the thoracolumbar junction or in the lumbar spine, there may be sufcient retroperitoneal bleeding from the fracture that causes an ileus and subsequent dehydration. It may be difcult to regulate pain medication in the elderly person with multiple co-morbidities in the acute emergency department setting. Long-acting and potent narcotics should be avoided, because side effects may be more common and less well tolerated in the elderly. Bracing can be useful for pain control if tolerated by the patient. Further immobilization with bedrest can lead to worsened osteopenia and pulmonary complications and should be avoided. Treatment of acute fractures should include institution of prophylactic medical measures to minimize further bone loss. Surgical management of these fractures is uncommon, especially because it is often fraught with complications. Indications for surgery include persistent or progressive neurologic decit, progressive deformity, and intractable pain. Surgical xation in the osteoporotic spine is complicated by poor bone stock; the use of bone cement to augment screw purchase may be considered, although some argument exists about whether U.S. Food and Drug Administration (FDA) approval is available for polymethyl methacrylate in this circumstance. Segmental instrumentation further decreases the forces at any one level; sublaminar wires have been used in this way to maximize the area of xation to the spine.19 The greatest care must be used to prevent a cheese slicer effect of the wire on the porotic lamina. Laminar hooks alone are associated with increased pull-out and laminar fracture rates in the osteoporotic spine. Pedicle screws confer the most rigid xation in the spine. Because the pedicle cortex is thinned in osteoporosis, pedicle screw purchase is enhanced by using the maximal screw diameter possible without breech.5 If necessary, pedicle screws may be supplemented by hooks at the same or adjacent levels; this provides a construct with the highest pull-out strength.17 However, the surgeon must consider the problem of subsequent transitional disease at a relatively early stage with this rigid xation. Vertebroplasty or vertebral compression fracture injection with polymethyl methacrylate is emerging as a nonoperative technique for pain management in selected patients. Such augmentation of a fractured osteoporotic vertebral body, a technique known as vertebroplasty (Fig. 332), may reduce exion-extension and lateral loading compliance by more than 20%, yielding a stiffer vertebral body with greater compressive strength.41 Clarication

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FIGURE 332. Vertebroplasty. A, A trephine is inserted transpedicularly into the posterior aspect of the fractured vertebral body. B, Cement injection lls the fractured vertebra, with the intent of conferring immediate stability to the fracture.

Presentation

should be obtained from the FDA before embarking on this procedure. Success rates higher than 90% have been reported with short-term follow-up.2 Pain may be reduced because of stabilization of microfractures in the vertebral body, because of load sharing by the cement, or because of cauterization of local nociceptive nerve endings.41 The condition of the posterior cortex of the vertebral body must be ensured before vertebroplasty; bone cement extravasation into the spinal canal can be disastrous. Injection alone cannot reduce kyphotic angulation of a vertebral compression fracture. To address this problem, another procedure is being investigated. In kyphoplasty, percutaneous delivery of a balloon to the fracture site to lift a collapsed vertebra into reduction is followed by vertebroplasty. Use of a nonthermally curing, biodegradable, injectable substance, such as calcium phosphate, for vertebral augmentation instead of polymethyl methacrylate is an area of active research.1

ANKYLOSING SPONDYLITIS

zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz A rheumatologic disorder belonging to the family of seronegative spondyloarthropathies, ankylosing spondylitis is an inammatory disease that leads to bilateral sacroiliitis and cephalad-progressing spinal ankylosis. There may be variable expression of extraspinal manifestations, including iridocyclitis, urethritis, aortitis, pulmonary apical brosis, aortic valve insufciency, cardiac conduction defects, and multiple arthralgias, especially in the hips and shoulders. The condition, also called Marie-Strumpell disease, occurs in less than 2% of people in the general population. There is a familial predilection with a strong inheritance association with the presence of the HLA-B27 histocompatibility antigen in about 90% of patients. Ankylosing spondylitis has been reported in men more than twice as frequently as in women, but it may be

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underreported in women because of a milder and slower progression of disease.9 Patients typically develop low back pain initially in the third and fourth decades. Anti-inammatory medication may provide some symptomatic relief, but in patients with full expression of the disease, inexorable spinal fusion progresses through the years from a caudal to cephalad direction. The enthesopathy causes calcication of the anulus brosus, anterior longitudinal ligament, posterior longitudinal ligament, ligamentum avum, and interspinous ligament, creating a squaring appearance of the vertebral bodies on plain radiographic imaging. Bone deposition progresses such that owing syndesmophytes eventually link adjacent vertebral bodies and nally create the radiographic abnormality known as the bamboo spine (Fig. 333A). In addition to pain management, proper conservative care in the early stages of this disease includes counseling on posture, avoiding pillows beneath the head or legs during sleep, and avoiding periods of lying totally at in bed. Ankylosis of the exed cervical and lumbar spine with loss of lordosis may lead to chin-on-chest and forwardbending xed deformities with severe functional disability, such as an inability to observe trafc lights or difculty opening the mouth, leading to nutritional depletion. Rib articulations with the thoracic spine and sternum also become involved in ankylosing spondylitis. Fusion of these joints leads to decreased chest wall expansion during inspiration, and restrictive lung disease can ensue in severe cases. Limited chest wall expansion during maximal inspiration is the most specic diagnostic measure for ankylosing spondylitis. Pulmonary complications are common after operative and nonoperative management of spinal fracture in these patients.11, 20, 35, 37, 38, 40 Despite increased bony deposition in the soft tissues about the spine, vertebral bone density decreases, with measurable osteopenia throughout the spine even in the early stages.30 This secondary form of osteoporosis may be a result of increased vascularity concordant with the inammatory process. The surgeon must not be confused by the fact that the process occasionally may extend partially up the spine from the sacroiliac joints and stop or, uncommonly, manifest with skip areas of ankylosis in the spine. Ankylosis often extends through the subaxial cervical spine, but the atlantoaxial and occipitocervical articulations may retain movement. Because these articulations may be the only mobile spinal joints in patients with extensive disease, they may experience increased shear forces. They may further be subject to chronic synovitis due to the underlying disease, becoming hypermobile and unstable. Traumatic atlantoaxial dislocation or occipitocervical dissociation, occasionally with associated odontoid fracture, is more common in these patients.3, 23, 33, 40 Patients with ankylosing spondylitis are predisposed to traumatic spinal fracture because of the increased stiffness and the decreased bone density of the spine. Long segments of fused vertebral levels lack discal and ligamentous energy-absorbing capability. Instead, applied traumatic moments have longer lever arms to act on the fused spine. The thinned bone has lower resistance to failure.

Low-energy injury may lead to fracture in this scenario, even with only physiologic loading. Traumatic spinal injury in ankylosing spondylitis is often from a hyperextension mechanism and most often involves the cervical spine (see Fig. 333B), although the mechanism may carry through to the thoracic and lumbar areas as well.20, 38, 40 Neurologic decit is common, and mortality rates may be as high as 50%.* Plain radiographic evaluation of the ankylosed spine after trauma is difcult because bony sclerosis from healing stress fractures and abundant bony syndesmophytes can obscure minimally displaced fractures.20 Increased suspicion for occult fracture must be maintained in the patient with ankylosing spondylitis who sustains trauma, because delayed diagnosis may lead to progressive spinal deformity and neurologic decit.13, 14 Tomography20 and CT evaluation are useful,38 and sagittal and coronal CT reconstructions can help avoid missing a transverse plane fracture. Triple-phase bone scanning may help localize an occult fracture. MRI may be the most sensitive method for evaluating traumatic injury in the ankylosed spine, with intramedullary edema and surrounding hematoma being indicators of acute fracture.14, 21 Fractures are often transdiscal, with or without vertebral body involvement, and associated posterior element fracture is common.25 The injury pattern of the long, fused spinal column mimics that in a long bone in which a transverse fracture occurs across its entire diameter; in the spine, the fracture occurs across the anterior, middle, and posterior columns. Immobilization of the spine-injured patient with ankylosing spondylitis differs from the norm in that signicant axial traction and straightened positioning should be avoided in favor of the preinjury position. These patients should be immobilized in the position of their chronic deformity with minimal change enacted. Iatrogenic displacement of a minimally displaced fracture can lead to spinal cord injury with paraplegia or quadriplegia if a chronically kyphotic cervical spine is forcibly altered into extension.15, 25, 40 Disimpaction of these fractures may further lead to motion at the fracture site and epidural hematoma formation, a complication indigenous to this disease. Halo management of minimally displaced fractures must therefore preserve the pretrauma deformity. Custom-t halo vests are often required. Nursing care may be complicated by chin-on-chest deformity, but pulmonary toilet remains critical in these patients, who may have preexisting pulmonary compromise. Nonoperative management of fractures in patients with ankylosing spondylitis has been attempted for some nondisplaced fractures with no neurologic decit. Prolonged bedrest with minimal traction, hard collar, or halo vest immobilization has been advocated for nondisplaced fractures.16, 20, 35, 40 Nevertheless, nonunion and neurologic deterioration have been observed with the use of such conservative measures in some of these patients.6, 11, 15, 35, 40 Cervical spinal fractures in ankylosing spondylitis often involve anterior and posterior column injuries, making the injury unstable and predisposing nonoperative treatment to failure. Operative management
*See references 6, 11, 13, 16, 20, 24, 35, 37, 38, 40.

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FIGURE 333. Ankylosing spondylitis. A, B, Anteroposterior (AP) and lateral radiographs of the cervical spine reveal the owing syndesmophytes and bony ankylosis of severe ankylosing spondylitis in this 68-year-old man. C, On the lateral cervical spine radiograph of the same patient 1 month later after a fall from a standing height, notice the shear fracture through the C6 vertebral body. D, E, Sagittal and axial computed tomography cuts reveal a transosseous fracture pattern involving all three columns, as well as an acute kyphotic angulation of the spine with retrolisthesis. Because of three-column involvement and concerns about screw purchase in osteoporotic bone, anterior and posterior cervical fusions with instrumentation and autologous bone graft were performed, and an adjunctive halo was used in the postoperative period. F, G, AP and lateral postoperative radiographs reveal a reduced fracture with lateral mass screws and plates posteriorly and an anterior plate and vertebral body screws.

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CHAPTER 33 Fractures in the Stiff and Osteoporotic Spine

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may therefore be preferred in many cases of spinal fracture in the setting of ankylosing spondylitis, especially in the presence of wide fracture displacement, progressive neurologic decit, a large epidural hematoma, or severe deformity that could complicate pulmonary rehabilitation and make difcult the tting of external bracing. Posterior approaches are often preferred in the thoracic spine because of coexisting pulmonary compromise from restrictive lung disease and in the cervical spine because anterior exposure may be difcult as a result of exaggerated cervicothoracic kyphosis.37 The posterior approach also allows greater exposure for longer segmental fusions. Inclusion of more points of xation to the spine is important to decrease the stress at any one vertebral level in an already osteoporotic spine.37 If an anterior procedure is desired because of a need for anterior decompression, a posterior fusion is usually added because of the tenuous xation achievable in the osteoporotic vertebral bodies anteriorly (see Fig. 333D). Extreme care must be used with intraoperative positioning to prevent exaggeration of correction; intraoperative neurophysiologic monitoring is often helpful in these situations. Hook placement in posterior thoracic fusions is difcult because of ossication of the ligamentum avum. Transverse process hooks, pedicle screws, and spinous process wires may be easier forms of instrumentation in this setting, although the latter instrument is much weaker and less secure. Similarly, sublaminar wires in the cervical spine would require excision of the calcied ligamentum; instead, lateral mass plates, pedicle screws, and interspinous wires are options. Epidural hematoma formation is more common after trauma in patients with ankylosing spondylitis and has been reported in 20% of these injuries.20, 38 An epidural hematoma must be suspected when neurologic deterioration occurs, especially when such deterioration follows an initial decit-free period. Spinal cord compression from an epidural hematoma may rarely be

further exacerbated by traumatic disc herniation in these patients.35 A different but related condition rst described in 1987, the syndrome of synovitis, acne pustulosis, and hyperostosis osteitis (SAPHO), represents another condition that may lead to spinal ankylosis. With SAPHO syndrome, syndesmophytes link adjacent vertebrae, forming long columns predisposed to fracture. Sacroiliitis may be present as well. Although similar to spondyloarthropathy in these ways, the spinal ankylosis in SAPHO syndrome does not extend from the sacrum cephalad and does not have similar extraspinal manifestations. There is no association with HLA-B27 antigenicity. Associated ndings instead include arthro-osteitis of the sternoclavicular and costosternal joints and skin manifestations of palmoplantar pustulosis, psoriasis, and severe acne.10 Cervical spinal fracture has been reported with a hyperextension injury pattern similar to that seen in ankylosing spondylitis. Nonoperative treatment for nondisplaced fracture has been successful.10

DIFFUSE IDIOPATHIC SKELETAL HYPEROSTOSIS

zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz Another disorder of idiopathic spinal ankylosis is diffuse idiopathic skeletal hyperostosis (DISH). With a slightly higher incidence in men than women, DISH occurs in people older than 50 years, with a prevalence approaching 10% to 20%.4, 39 Unlike degenerative spondylosis with arthrosis of the facet and uncovertebral joints, which can lead to signicant osteophyte growth but rarely intervertebral fusion, DISH results in an anterolateral fusion mass across many levels.12 Also known as ankylosing hyperostosis or Forestier disease, DISH is diagnosed when there is anterolateral intervertebral fusion extending across at least four adjacent levels, preservation of disc height without signicant disc disease, and absence of sacroiliac joint or apophyseal joint degeneration and fusion (Fig. 334A).39 Patients with DISH exhibit less spinal osteoporosis compared with ankylosing spondylitis, and peripheral skeletal involvement is usually absent in DISH.29 Patients usually have some mild, chronic middle and lower back pain symptoms, with a mild decrease in exion and extension; marked deformity as in ankylosing spondylitis does not typically occur. There may be skip areas in the fusion mass of DISH, unlike ankylosing spondylitis. Although spinal ankylosis in DISH does not necessarily extend from the sacrum up through the cervical spine, as in severe cases of ankylosing spondylitis, long segmental vertebral fusions do create stiff areas with long lever arms through which destructive forces may act. These areas may be susceptible to low-energy hyperextension injury, resulting in three-column injury.3, 18 The posterior element fracture and anterior spinal widening pattern characteristic of distraction-extension injuries may therefore occur after trauma in patients with DISH (see Fig. 334B).7, 18, 22, 27

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FIGURE 33-3 Continued.

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FIGURE 334. Diffuse idiopathic skeletal hyperostosis. A, B, Anteroposterior and lateral cervical spine radiographs of a patient with diffuse idiopathic skeletal hyperostosis (DISH). There is an anterolateral fusion mass from C2 to C5, but the facet joints, uncovertebral joints (white arrow), disc spaces, interspinous process ligaments, and ligamentum avum are uninvolved. C, Lateral radiograph of the lumbar spine in a different patient after a car accident reveals a distraction extension injury at the L2L3 level, immediately below a long segment of DISH in the thoracolumbar spine. (A, From Meyer, P.R., Jr. Clin Orthop 359:4957, 1999.)

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As in ankylosing spondylitis, the risk for neurologic decit and post-traumatic mortality is high.3, 18, 22, 29, 31 Delay in diagnosis may contribute to the development of secondary neurologic deterioration.8, 18 The hyperextension injury in the setting of DISH more often involves fracture through the vertebral body; hyperextension injuries in ankylosing spondylitis more often are transdiscal in nature. Plain radiographs, CT imaging, and MRI may be useful in delineating the injury.7, 27 Management of hyperextension fractures associated with DISH follows principles similar to those for management of ankylosing spondylitisassociated fractures. Segmental xation is useful to avoid overdistraction of the anteriorly decient spinal column and to stabilize the posterior column.7, 34 Usually, the bone quality in DISH is far better

than in ankylosing spondylitis and, as a result, is much more tolerant and responsive to alternative forms of xation.
REFERENCES 1. Bai B; Jazrawi, L.M.; Kummer, F Spivak, J.M. The use of an .J.; injectable, biodegradable calcium phosphate bone substitute for the prophylactic augmentation of osteoporotic vertebrae and the management of vertebral compression fractures. Spine 24:15211526, 1999. 2. Barr, J.D.; Barr, M.S.; Lemley, T.J.; McCann, R.M. Percutaneous vertebroplasty for pain relief and spinal stabilization. Spine 25:923 928, 2000. 3. Bernini, P.M.; Floman, Y.; Marvel, J.P., Jr.; Rothman, R.H. Multiple thoracic spine fractures complicating ankylosing hyperostosis of the spine. J Trauma 21:811814, 1981.

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CHAPTER 33 Fractures in the Stiff and Osteoporotic Spine 4. Bloom, R.A. The prevalence of ankylosing hyperostosis in a Jerusalem populationWith a description of a method of grading the extent of disease. Scand J Rheumatol 13:181189, 1984. 5. Brantley, A.G.V.; Mayeld, J.K.; Clark, K.R. The effects of pedicle screw t: An in vitro study. Spine 19:17521758, 1994. 6. Broom, M.J.; Raycroft, J.F Complications of fractures of the cervical . spine in ankylosing spondylitis. Spine 13:763766, 1998. 7. Burkus, J.K.; Denis, F Hyperextension injuries of the thoracic spine . in diffuse idiopathic skeletal hyperostosis: Report of 4 cases. J Bone Joint Surg Am 76:237243, 1994. 8. Colterjohn, N.R.; Bednar, D.A. Identiable risk factors for secondary neurologic deterioration in the cervical spine-injured patient. Spine 20:22932297, 1995. 9. Cooper, C.; Carbone, C.; Michet, C.J.; et al. Fracture risk in patients with ankylosing spondylitis: A population-based study. J Rheumatol 21:18771882, 1994. 10. Deltombe, T.; Nisolle, J.F Boutsen, Y.; et al. Cervical spinal cord .; injury in SAPHO syndrome. Spinal Cord 37:301304, 1999. 11. Detwiler, K.N.; Loftus, C.M.; Godersky, J.C.; Menezes, A.H. Management of cervical spine injuries in patients with ankylosing spondylitis. J Neurosurg 72:210215, 1990. 12. Fardon, D.F Odontoid fracture complicating ankylosing hyperostosis . of the spine. Spine 3:108112, 1978. 13. Farmer, J.; Vaccaro, A.; Albert, T.J.; et al. Neurologic deterioration after cervical spinal cord injury. J Spinal Disord 11:192196, 1998. 14. Finkelstein, J.A.; Chapman, J.R.; Mirza, S. Occult vertebral fractures in ankylosing spondylitis. Spinal Cord 37:444447, 1999. 15. Fox, M.W.; Onofrio, B.N. Neurological complications of ankylosing spondylitis. J Neurosurg 78:871878, 1993. 16. Graham, B.; Van Peteghem, P.K. Fractures of the spine in ankylosing spondylitis: Diagnosis, treatment, and complications. Spine 14:803 807, 1989. 17. Hasegawa, K.; Takahashi, H.E.; Uchiyama, S. An experimental study of a combination method using a pedicle screw and laminar hook for the osteoporotic spine. Spine 22:958963, 1997. 18. Hendrix, R.W.; Melany, M.; Miller, F Rodgers, L.F Fracture of the .; . spine in patients with ankylosis due to diffuse idiopathic skeletal hyperostosis: Clinical and imaging ndings. AJR Am J Roentgenol 162:899904, 1994. 19. Hu, S.S. Internal xation in the osteoporotic spine. Spine 22:43S 85S, 1997. 20. Hunter, T.; Dubo, H. Spinal fractures complicating ankylosing spondylitis: A long-term follow-up study. Arthritis Rheum 26:751 759, 1983. 21. Iplikcioglu, A.C. Magnetic resonance imaging in cervical trauma associated with ankylosing spondylitis: Report of two cases. J Trauma 36:412413, 1994. 22. Israel, Z.; Mosheiff, R.; Gross, E.; et al. Hyperextension fracturedislocation of the thoracic spine with paraplegia in a patient with diffuse idiopathic skeletal hyperostosis. J Spinal Disord 7:455457, 1994.

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23. Kaplan, S.L.; Tun, G.C.; Sarkarati, M. Odontoid fracture complicating ankylosing spondylitis: A case report and review of the literature. Spine 15:607610, 1990. 24. Karasick, D.; Schweitzer, M.E.; Abidi, N.A.; Cotler, J.M. Fractures of the vertebra with spinal cord injuries in patients with ankylosing spondylitis. AJR Am J Roentgenol 165:12051208, 1995. 25. Lane, J.M. Osteoporosis: Medical prevention and treatment. Spine 22:32S37S, 1997. 26. Lee, Y.L.; Yip, K.M. The osteoporotic spine. Clin Orthop 323:9197, 1996. 27. Leltir, P.X.; Saulet, A.; LeGars, L.; et al. Hyperextension vertebral body fractures in diffuse idiopathic skeletal hyperostosis: A case of intravertebral uidlike collections on MR imaging. AJR Am J Roentgenol 173:16791683, 1999. 28. Melton, L.J., III. Epidemiology of spinal osteoporosis. Spine 22:2S11S, 1997. 29. Meyer, P.R., Jr. Diffuse idiopathic skeletal hyperostosis in the cervical spine. Clin Orthop 359:4957, 1999. 30. Mitra, D.; Elvins, D.M.; Speden, D.J.; Collins, A.J. The prevalence of vertebral fractures in mild ankylosing spondylitis and their relationship to bone mineral density. Rheumatology 39:8589, 2000. 31. Mody, G.M.; Charles, R.W.; Ranchord, H.A.; Rubin, D.L. Cervical spine fracture in diffuse idiopathic skeletal hyperostosis. J Rheumatol 15:129131, 1991. 32. Myers, E.R.; Wilson, S.E. Biomechanics of osteoporosis and vertebral fracture. Spine 22:25S31S, 1997. 33. Ozgocmen, S.; Ardicoglu, O. Odontoid fracture complicating ankylosing spondylitis. Spinal Cord 38:117119, 2000. 34. Paley, D.; Schwartz, M.; Cooper, P.; et al. Fractures of the spine in diffuse idiopathic skeletal hyperostosis. Clin Orthop 267:2232, 1991. 35. Rowed, D.W. Management of cervical spinal cord injury in ankylosing spondylitis: The intervertebral disk as a cause of cord compression. J Neurosurg 77:241246, 1992. 36. Silva, M.J.; Keaveny, T.M.; Hayes, W.C. Load sharing between the shell and centrum in the lumbar vertebral body. Spine 22:140150, 1997. 37. Taggard, D.A.; Traynelis, V.C. Management of cervical spine fractures in ankylosing spondylitis with posterior xation. Spine 25:2035 2039, 2000. 38. Tico, N.; Ramon, S.; Garcia-Ortun, F et al. Traumatic spinal cord .; injury complicating ankylosing spondylitis. Spinal Cord 36:349 352, 1998. 39. Utsinger, P.D. Diffuse idiopathic skeletal hyperostosis. Clin Rheum Dis 11:325351, 1985. 40. Weinstein, P.R.; Karpman, R.R.; Gall, E.P.; Pitt, M. Spinal cord injury, spinal fracture, and spinal stenosis in ankylosing spondylitis. J Neurosurg 57:609616, 1982. 41. Wilson, D.R.; Myers, E.R.; Mathis, J.M.; et al. Effect of augmentation on the mechanics of vertebral wedge fractures. Spine 25:158165, 2000.

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